COPD Flashcards

1
Q

What causes airway narrowing/obstruction?

A

muscle spasm
mucosal oedema
airway collapse due to loss of support
tumour or foreign body stuck in lumen

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2
Q

What are the 3 aspects that make up COPD?

A

chronic bronchitis
emphysema
small airway inflammation (respiratory bronchiolitis)

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3
Q

Define chronic bronchitis.

A

Cough productive of sputum on most days for 3 months of at least 2 successive years

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4
Q

How does chronic bronchitis come about?

A

Chronic irritation (cigarette smoke/atmospheric pollution) leads to a defensive increase in mucus production with increase in numbers of epithelial cells (esp. goblet cells). This gives a role in sputum production and increased tendency to infection

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5
Q

Is chronic bronchitis reversible or non-reversible obstruction?

A

non-reversible

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6
Q

What can cause small airway inflammation in COPD?

A

Goblet cell metaplasia, macrophage accumulation and fibrosis (scarring) around bronchioles may generate functional obstruction

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7
Q

Define emphysema.

A

Increase beyond the normal in the size of the airspaces distal to the terminal bronchiole without fibrosis

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8
Q

What types of emphysema are there?

A

centriacinar (centrilobular)
panacinar (whole lobule affected)
Other types can occur localised around scars in the lung

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9
Q

How is emphysema diagnosed?

A

Difficult to diagnose

CT scan used - shows changes in lung density

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10
Q

What is the “dilation” in emphysema due to?

A

loss of alveolar walls not an increase in normal space

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11
Q

What can be found in the lungs of smokers and urban dwellers?

A

Carbon pigmentation

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12
Q

How does emphysema impair respiratory function?

A
  • diminished alveolar surface area for gas exchange

- loss of elastic recoil so support of small airways is not apparent leading to tendency to collapse with obstruction

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13
Q

As COPD advances what does a decreased PaO2 lead to?

A
Dyspnoea and increased respiratory rate
Pulmonary vasoconstriction (and pulmonary hypertension)
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14
Q

What are the 3 main epidemiological factors that relate to the development of COPD?

A

Smoking
atmospheric pollution
Genetic factors

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15
Q

What is alpha1- anti-trypsin deficiency?

A

an autosomal dominant genetic condition
- deficiency in alpha1- anti-trypsin leads to an increased number of elastases (enzymes produced by neutrophils and macrophages) which leads to the destruction of elastic alveolar walls (emphysema)

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16
Q

How does tobacco smoke indirectly inhibit alpha1- anti-trypsin?

A

Tobacco smoke Increases number of neutrophils and macrophages in lungand slows transit of these cells. This promotes neutrophil degranulation releasing elastase which inhibits  1 antitrypsin

17
Q

What leads to mucous hypersecretion in chronic bronchitis?

A

Marker hypertrophy of mucous secreting glands and hyperplasia of goblet cells (caused by chronic inflammation from cigarette smoke)

18
Q

In emphysema, which immune cells show a chronic inflammation?

A

neutrophils, macrophages and CD8+ T cells

19
Q

How is COPD assessed?

A

Symptoms
spirometry - degree of airflow limitation
CXR - to exclude aditional diagnoses
risk of exacerbations

20
Q

What are the symptoms of COPD?

A
chronic symptoms 
daily productive cough 
progressive breathlessness 
wheeze 
infective exacerbation - increased cough with purulent sputum
21
Q

What are the signs of COPD?

A

tachyponea
use of accessory muscles
hyperinflation of chest
decreased chest expansion

22
Q

what are emphysematous bullae?

A

Large (>1cm) closed off air spaces with trapped air seen on CXR

23
Q

How is the severity of COPD expressed?

A

Mild - FEV1 50-80% off predicted
Moderate - FEV1 30-49% predicted
Severe - FEV1 <30% of predicted

24
Q

What are the non-pharmacological interventions for COPD?

A
stop smoking 
encourage exercise 
treat poor nutrition or obesity 
influenza & pneumococcal vaccinations 
pul rehab/ palliative care
25
Q

How is Mild COPD treated?

A

Salbutamol or ipratropium

26
Q

How is moderate COPD treated?

A

Ipratropium or salmeterol and inhaled beclometasone (corticosteroid)

27
Q

How is severe COPD treated?

A

Salmeterol and beclometasone and ipratropium and refer to specialist

28
Q

What is the treatment for an acute exacerbation of COPD?

A
ABCDE 
IV access (FBC,U&Es, blood culture)
O2 (88-92%) & ABG 
Oral prednisolone/ IV hydrocortisone 
Amoxicillin oral (if infective)
Nebulised Salbutamol (bronchodilator)
Physiotherapy to expel secretions
29
Q

What are the complications of COPD?

A
Respiratory failure (type 2)
Cor pulmonale (heart failure 2y to disease of the lung)